期刊
JOURNAL OF VIROLOGY
卷 79, 期 22, 页码 13974-13983出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.79.22.13974-13983.2005
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资金
- NIAID NIH HHS [K23 AI079394, K08 AI59390-01, U54 AI057160, K08 AI059390] Funding Source: Medline
- NIAMS NIH HHS [P30 AR048335] Funding Source: Medline
- PHS HHS [R01 A144157] Funding Source: Medline
The innate immune response, and in particular the alpha/beta interferon (IFN-alpha/beta) system, plays a critical role in the control of viral infections. Interferons alpha and beta exert their antiviral effects through the induction of hundreds of interferon-induced (or -stimulated) genes (ISGs). While several of these ISGs have characterized antiviral functions, their actions alone do not explain all of the effects mediated by IFN-alpha/beta. To identify additional IFN-induced antiviral molecules, we utilized a recombinant chimeric Sindbis virus to express selected ISGs in WN-alpha/beta receptor (IFN-alpha/beta R)(-/-) mice and looked for attenuation of Sindbis virus infection. Using this approach, we identified a ubiquitin homolog, interferon-stimulated gene 15 (ISG15), as having antiviral activity. ISG15 expression protected against Sindbis virus-induced lethality and decreased Sindbis virus replication in multiple organs without inhibiting the spread of virus throughout the host. We establish that, much like ubiquitin, ISG15 requires its C-terminal LRLRGG motif to form intracellular conjugates. Finally, we demonstrate that ISG15's LRLRGG motif is also required for its antiviral activity. We conclude that ISG15 can be directly antiviral.
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